Poster sessions P.1.a Basic and clinical neuroscience – Genetics and epigenetics P.1.a.002 The influence of childhood trauma, major depressive disorder and telomere length on HIV-associated neurocognitive disorders J. Womersley 1 *, G. Spies 1 , S. Malan-Müller 1 , G. Tromp 2 , S. Hemmings 1 , S. Seedat 1 1 University of Stellenbosch, Psychiatry, Cape Town, South Africa; 2 University of Stellenbosch, Biomedical Sciences, Cape Town, South Africa Background: HIV-associated neurocognitive disorders (HAND) continue to prevail in countries affected by HIV/AIDS, despite improved access to antiretroviral therapies. Previous research has suggested that this is in part due to the complex interactions between stress-related exposures and depression, which may aggravate the development of neurocognitive impairment [1,2]. This relationship is particularly relevant to sub-Saharan Africa, where HIV is most prevalent. The combination of HIVand stress- related exposure essentially produces a double burden of disease. Telomere length attrition is a marker of biological aging that has been independently associated with childhood trauma, depression and HAND. We therefore sought to investigate whether telomere shortening may act as a biomarker for HAND when examined in the context of childhood trauma and depression. Here we report on telomere length as a potential mediating factor between HAND and psychological stress. Methods: HIV-positive (n = 133) and negative women (n = 150) underwent a battery of neuropsychological tests to measure seven domains of cognitive function: motor skill, verbal fluency, attention and working memory, processing speed, learning, recall, and executive function, from which a global cognitive score was calculated. Study participants also completed the Childhood Trauma Questionnaire and the Centre for Epidemiological Studies Depression Scale. Quantitative polymerase chain reaction using primers specific to telomeric repeats and the reference gene human β-globin was performed on DNA extracted from peripheral blood mononuclear cells. Data were non-normally distributed according to a Shapiro-Wilk W test and were therefore subjected to an inverse hyperbolic sine transformation. Baseline differences in relative telomere length and neuropsychological parameters between HIV- positive and negative individuals were assessed using Welch’ s unequal variances t-test. The relationship between telomere length, cognitive function, childhood trauma and depression was probed using multiple linear regression models with age as a covariate. Data were analysed using the R statistical language, and an alpha value of less than 0.05 was deemed statistically significant. Results: HIV-positive individuals had significantly reduced relative telomere lengths (t(275.45) = 5.731, p < 0.0001) and self-reported higher levels of childhood trauma (t(262.59) = -7.671, p < 0.0001). Regression analysis revealed that including the interaction between childhood trauma and HIV status in the statistical model explained significantly more of the variance in telomere length ( p = 0.035). HIV status, childhood trauma, depression and telomere length individually did not affect cognitive function. However, the interaction of childhood trauma and depression explained significantly more of the variance in global cognitive scores across participants (p = 0.022). In contrast, including the interaction between depression and telomere length explained significantly more of the variance in global cognitive function in HIV positive individuals (p = 0.025). Conclusions: Our data suggest that HIV is associated with decreased telomere length and that the interaction between this biomarker and psychological ill health may influence cognitive status. The next step is to examine the relationship between longitudinal changes in telomere length and cognitive function to determine if telomere attrition is a cause or correlate of neurocognitive function in this study population. References [1] Spies, G., Fennema-Notestine, C., Cherner, M., Seedat, S., 2017. Changes in cognitive function in women with HIV function and early life stress. AIDS Care 29, 14–23. [2] Schouten, J., Su, T., Wit, F.W., Kootstra, N.A., Caan, M.W., Geursten, G.J., Schmand, B.A., Stolte, I.G., Prins, M., Majoie, C.B., Portegies, P., Reiss, P., AGEhIV Study Group, 2016. Determinants of reduced cognitive performance in HIV-1-infected middle-aged men on combination antiretroviral therapy. AIDS 30, 1027–1038. P.1.a.003 PDE7B, NMBR and EPM2A variants and schizophrenia: a case-control and pharmacogenetics study H. Kim 1 *, T.Y. Jun 1 1 The Catholic University of Korea St. Mary’ s Hospital, Neuropsychiatry, Seoul, South-Korea Background: Schizophrenia is a devastating psychiatric disease that affects about 1% of the population and ranks among the top 10 causes of disability worldwide [1]. In the last few decades, several association studies were performed in order to evaluate the impact of several genetic variations in specific candidate genes in the etiopathology of schizophrenia as well as in the antipsychotic response. We investigated the role of 8 single-nucleotide polymorphisms (SNPs) within 3 genes that could be potentially involved in the etiology of schizophrenia as well as in the antipsychotic response. They include phosphodiesterase 7B (PDE7B), neuromedin B receptor (NMBR) and epilepsy progres- sive myoclonus type 2A (EPM2A). To the best of our knowledge, these genes have been poorly investigated in studies of schizophrenia. Methods: Five hundred and seventy-three schizophrenia inpatients of Korean ethnicity and 560 healthy controls were genotyped for 2 PDE7B, 3 NMBR and 3 EPM2A polymorphisms. Differences in the allelic and genetic frequencies among healthy subjects and patients were calculated using the χ 2 statistics. Repeated measure ANOVAwas used to test possible influences of single-nucleotide polymorphisms on treatment efficacy. In case of positive findings, clinical and demographic variables were added as covariates, in order to investigate possible stratification bias. Results: The rs2717 and rs6926279 within the NMBR gene and rs702304 and rs2235481 within the EPM2A gene were associated with schizophrenia liability. More in detail, concerning the NMBR S577